Although mutations of several amino acid residues outside of the BB loop, such as 631H [16], 677R [20], [21], 713C [22], 715Tyr [14] and 753R [23], [24], [25], were reported to be indispensable for TLR2 signalling transduction and associated with tuberculosis, leprosy, staphylococcal infection or atopy risk, none of these residues was demonstrated to influence the interaction of the TLR2 TIR domain with MyD88, either directly or indirectly. This evidence concerns the gene MYD88 and leprosy.